FELINE PANLEUCOPENIA
NICOLA DECARO AND CANIO BUONAVOGLIA
Department of Veterinary Public Health, Faculty of Veterinary Medicine of Bari, Valenzano (Bari), Italy
Feline panleukopenia virus (FPLV) is a parvovirus closely related to CPV2, exhibiting the same virion structure and physico-chemical properties.
Unlike CPV2, which causes haemagglutination at wide pH values and in erythrocytes of various species, FPLV is able to agglutinate pig red blood cells only at pH values lower than 6.0. At the genetic level, FPLV has a nucleotide identity to CPV2 of more than 98%, differing only in six to seven amino acid residues of the VP2 protein. These mutations may be responsible for the different haemagglutination properties and for the host-receptor specificity. FPLV can replicate in vitro on cell lines of feline origin but not in canine cells, inducing the appearance of intranuclear inclusion bodies; however, a cytopathic effect is not always evident. Apart from CPV2, there are wild-carnivore parvoviruses of the feline parvovirus subgroup that are more closely related to FPLV: namely mink enteritis virus (MEV), raccoon parvovirus (RPV) and blue fox parvovirus (BFPV). Currently, these viruses are considered host variants of FPLV rather than separate parvovirus species.EPIDEMIOLOGY
FPLV has been known since the first decades of the 20th century and is now widespread in all parts of the world, including Europe. The natural host is the domestic cat (Felis silvestris catus), and kittens aged between 6 and 14 weeks are highly susceptible to FPLV infection. FPLV is also frequently observed in newborn kittens as a consequence of prenatal infections. FPLV can also infect wild felids (including large felids) and members of the families Mustelidae and Procyonidae. Active virus infection was demonstrated in a free-ranging Iberian lynx (Lynx pardi- nus) in Spain(7) and in a Eurasian lynx (Lynx lynx) reintroduced into Switzerland*13).
FPLV antibodies were detected in the Iberian lynx in Spain*7) and in the Eurasian lynx in Sweden*14), as well as in wildcats *Felis silvestris) in Portugal*5), Scotland*15), France, Switzerland and Germany*16). FPLV antigens were also detected by immunohistochemistry in European hedgehogs *Erinaceus europaeus) affected by acute gastroenteritis; the source of infection was suspected to be domestic cats*17). Due to the close relationship between FPLV and CPV2, investigations based on antibody detection are not useful to determine the specificity of the immune response and thus to discriminate between antibodies raised against FPLV and those induced by CPV2. Consequently, parvovirus antibodies detected in some European wild carnivores *see the section on canine parvoviral enteritis) may have been actually induced by FPLV instead of CPV2. The recent detection of the CPV2 variants in domestic and non-domestic felids further complicates the epidemiology of carnivore parvoviruses in wildlife, considering that these viruses are responsible for many feline panleucopenia outbreaks in felids.FPLV is shed predominantly in the faeces, but urine and saliva can contain a certain amount of infectious particles as a consequence of the high-titre viraemia. Pregnant queens can infect their offspring through vertical transmission. In postnatal infections, susceptible kittens are infected mainly by the oronasal route.
PATHOGENESIS, PATHOLOGY AND IMMUNITY
After a primary replication in the regional lymphoid tissues, the virus spreads through the bloodstream to target tissues, i.e. the epithelium of the intestinal crypts, the stem cells of bone marrow, and the lymphoid cells. FPLV pathogenesis is similar to that of CPV2, but the effects of FPLV replication in the bone marrow are of much greater severity in comparison with CPV2. In prenatal infections, the virus is transmitted vertically by the infected queen to the fetuses and rapidly spread to the Purkinje cells of the cerebellum, causing abortion or, more frequently, birth of kittens with cerebellar hypoplasia, hydrocephalus and retinal degeneration. Like CPV2, FPLV induces an early immune response, with antibody titres peaking shortly after the onset of clinical signs, and recovered cats probably have a life-long protection against reinfection.
Gross lesions observed during FPLV infections are haemorrhagic or fibrinonecrotic enteritis, enlargement of lymph nodes and atrophy of the thymus. The bone marrow can be gelatinous and liquefactive. Microscopic changes include necrosis of the mucosa of small intestine, with presence of intranuclear inclusion bodies in the epithelium, myeloid destruction in the bone marrow and depletion of lymphocytes in the lymphoid tissues.
There are no reports on the clinical signs and pathology of FPLV infections in European free-ranging felids. However, two fatal cases of FPLV infection were described in two captive felines, a 1.5-year-old Eurasian lynx and a 3.5-month-old European wildcat, living in the same wildlife park in Germany*18). The gross lesions and microscopic changes were undistinguishable from those usually observed in domestic cats, and the source of infection was proven to be the feral cat population living in the park.
By sequence and phylogenetic analysis of the VP2 protein gene, the virus was found to be very closely related to a typical FPLV strain detected in France.
CLINICAL SIGNS AND TREATMENT
Postnatal infections can have a subclinical or an inapparent course, mainly in adult cats, or lead to peracute forms with sudden death, especially in young kittens. The incubation period can vary between 2 and 10 days, and clinical signs are usually characterized by anorexia, depression, abdominal pain, vomiting and fluid — sometimes bloody — diarrhoea. Fever can be succeeded by hypothermia, especially in the terminal stages of the disease. WBC counts may be particularly low, reaching values less than 500 leucocytes/ μl of blood. Unlike CPV2, which may cause only acute lymphopenia with normal neutrophil counts, FPLV induces the reduction of all WBC, including neutrophils, as a consequence of the bone marrow involvement. Respiratory distress and nasal discharge may appear as a consequence of secondary bacterial infections. The outcome of prenatal infections depends on the stage of pregnancy when infection is acquired.
In the early stages of pregnancy, embryonic death and resorption are frequent, whereas abortion or fetal mummification is more common in the later stages. Prenatal infections occurring in the last 2 weeks of pregnancy are usually associated with the birth of kittens affected by neurological signs consisting of hypermetria, dysmetria and incoordination. Neurological disorders can also occur in infected kittens aged less than 2 weeks.Treatment of FPLV infection in infected carnivores is supportive only, based on fluid therapy to rehydrate and restore electrolyte balance and antibiotics for secondary bacterial infections. Prognosis is generally poor.
DIAGNOSIS
FPLV infection should be suspected in the presence of a severe leucopenia, especially in young animals. Confirmatory tests are the same as those used for detection of CPV2 infection. Recently, a MGB probe assay for discrimination between CPV2 variants and FPLV was developed, which is potentially useful considering the increasing number of feline infections caused by the canine viruses1-19).
MANAGEMENT, CONTROL AND REGULATIONS
FPLV prophylaxis in domestic cats is based on the systematic vaccination of kittens after the wane of MDA immunity using killed or MLV vaccines. According to the relatively high frequency of detection of the CPV2 variants in felids with clinical signs of feline panleucopenia, combined FPLV/CPV2 vaccines should be developed. Although this strategy is hardly applicable to free- ranging wildlife, vaccination of felids to be reintroduced into the wild is recommended. In fact, release into the wild of nondomestic felids bred in captivity would bring about a high risk of introducing of FPLV infection to free-ranging wildlife populations. FPLV can infect a wide range of carnivores but it is not a human pathogen.